Abstract

The selective suppression of flicker response from LWS cones has been investigated with two approaches. One approach has emphasized the use of light-adaptation conditions, and the other has emphasized the use of dark-adaptation conditions. In both cases, stimuli are arranged to restrict or exceed the ability of adaptation processes to maintain an afferent flicker response, and long-wavelength stimuli are used to overload spectrally opponent processes. By integrating these two approaches, this study shows that diverse manifestations of flicker response suppression can be closely related mechanistically. For instance, the steep flicker TVI slopes that resulted from superimposing temporally modulated (100% contrast) test stimuli on flashed backgrounds corresponded to the disappearance of flicker that resulted from increasing the time-averaged illuminance of temporally modulated stimuli (contrast x<100%) that were flashed alone in an otherwise dark field. For the stimulus parameters of this study, flicker response suppression was more evident for small (19′ diameter) than for large (1° diameter) stimuli. However, flicker response suppression was elicited reliably for both sizes by adding a spatially coincident short-wavelength stimulus to the interstimulus interval between presentations of the long-wavelength stimuli. By showing that temporal contrast can be treated as an independent variable for an important set of test/background stimulus combinations, the results of this study make it possible to investigate the means by which changes of contrast gain help to maintain flicker response as assessed in a conventional flicker TVI paradigm. The reduced degree of suppression for relatively large stimuli probably is related to the increased action of spatially extensive contrast gain-control processes. These contrast gain-control processes might not act independently of spectrally opponent processes.

A blood sample from subject MAW was kindly analyzed by Jay and Maureen Neitz using polymerase chain reaction (PCR) methodology to estimate (a) the ratio of LWS/MWS cone pigment genes and (b) the ratio of first to downstream genes.26 Subject MAW had 50% LWS genes and 67% downstream genes. This is consistent with two possibilities: (1) one of her gene arrays has 1 LWS and 2 MWS genes, while the other has 2 LWS and 1 MWS gene, or (2) one of her gene arrays has 1 LWS and 3 MWS genes, while the other has 2 LWS genes. At least 8% of normal males have multiple LWS genes in their single gene array [S. A. Sjoberg, M. Neitz, S. D. Balding, J. Neitz, “L-cone pigment genes expressed in normal colour vision,” Vision Res. 38, 3213–3219 (1998)], implying that at least ∼15% of normal females have multiple LWS genes in one or the other of their two gene arrays.

If one of subject MAW’s gene arrays has 1 LWS and 2 MWS genes while the other has 2 LWS and 1 MWS gene (see Ref. 27), then the probability of subject MAW being a deutan carrier is less than roughly 49%=0.12/[(0.15)(1-0.12-0.04)+0.12], since ∼12% of women of European ancestry are deutan carriers and ∼4% are protan carriers [L. T. Sharpe, A. Stockman, H. Jagle, J. Nathans, “Opsin genes, cone photopigments, color vision, and color blindness,” in Color Vision: From Genes to Perception, K. Gegenfurtner, L. T. Sharpe, eds. (Cambridge U.P., Cambridge, UK, 1999), pp. 3–51]. If one of subject MAW’s gene arrays has 1 LWS and 3 MWS genes while the other has 2 LWS genes, then the probability of subject MAW being a deutan carrier is 100%. Estimating the overall probability depends on knowing the relative likelihood of the two possibilities.

Although the presence of more than 2 LWS genes is by itself consistent with a substantial probability that subject MAW is color normal (see Refs. 27 and 28), her discrimination data suggest that she indeed is a carrier [J. Pokorny, V. C. Smith, G. Verriest, “Congenital color vision defects,” in Congential and Acquired Color Vision Defects, J. Pokorny, V. C. Smith, G. Verriest, A. J. L. G. Pinckers, eds. (Grune & Stratton, New York, pp. 180–241)]. For females who know that their father and maternal grandfather have normal color vision, and who do not exhibit Schmidt’s sign, the probability of being a carrier is ∼4% (=12%/3). The probability would be less if the color vision of several brothers or maternal uncles were known to be normal. Subject MAW, who did not exhibit Schmidt’s sign, knew the color vision status of only one relative, a color-normal maternal uncle.

The requisite frequencies for subjects JRC and MRK decreased simultaneously, from 17 to 15 Hz for JRC and from 15 to 13 Hz for MRK. However, the calibration was unaltered. This suggests that some change in the environment (e.g., more light exposure in early springtime) was responsible. The other two subjects were not being tested at the time.

A smaller step size was not used for two reasons. A smaller step size would have increased the duration of the test sessions, which in some cases already exceeded 3 hours. In addition, a smaller step size would have resulted in more-prolonged exposure to suprathreshold flicker.

For each subject, the temporal frequency was chosen to elicit a middle branch. Increasing temporal frequencies by as little as 2 Hz caused flicker thresholds for all temporal contrasts to lie on the equivalent of the upper branch. Reducing temporal frequency caused the range of temporal contrasts corresponding to multiple flicker thresholds to shift to lower temporal contrasts. These results are consistent with previously published data obtained for 13′-diameter stimuli centered within surrounding annuli.4

This was true even for subject JRC (Fig. 3, upper left), for whom the derived and the measured flicker TVI did not share the same set of background illuminances. This disparity resulted from inappropriate corrections to computer lookup tables following a small discrete (1 gear-tooth slippage) rotational translation of the neutral density wedge in the test channel.

This observation was made on the basis of many between-session comparisons for subject JRC and two within-session comparisons for subject MRK. Subject JMG could not serve as a subject for experiments involving the exchange procedure because alternating the short- and long-wavelength lights caused her to become dizzy.

When a 3.26-log-td exchange stimulus was used, light-level limitations precluded measurement of the reappearance threshold.

At background illuminances where the 660-nm flicker TVI curve rises steeply, the time-averaged 540-nm:660-nm test/background combination is metameric to a wavelength appreciably less than 600 nm. For subject JRC, the 660-nm:540-nm log threshold difference typically overshot the MWS-cone isolation line at background illuminances corresponding to the onset of the upper branch of the 660-nm TVI curve. At higher background illuminances, the 660-nm:540-nm differences retreated to values similar to those in Fig. 7. Subject JRC was tested at 17 Hz. (His data are not graphed because the period between test wavelength changes was less than 3 min whenever background illuminance was unchanged). A temporary overshoot would be expected if there were a narrow range of background illuminances for which MWS-cone-mediated flicker response were isolated using 660-nm tests but for which LWS-cone-mediated flicker response continued to predominate with 540-nm tests.

On the basis of data from one subject (JMG), it appears that the 660-nm:540-nm log-threshold difference depends on temporal frequency. Overshoots of the MWS cone isolation line (see note 39) seem more likely to occur for 15- or 17-Hz stimuli than for 13-Hz stimuli. In addition, there was evidence that the slope of the 660-nm:540-nm log-threshold difference versus background-illuminance curve tended to increase as temporal frequency increased from 13 to 17 Hz. The asymptotic 660-nm:540-nm log-threshold differences may have increased also. For subject MAW, who was tested at 14 Hz only, the degree of MWS-cone isolation appeared incomplete. At dim background illuminances, subject MAW’s 660-nm:540-nm log-threshold difference sometimes appeared to be dominated by LWS cones and sometimes appeared to be better described by V(λ).

It is not known why small but apparently systematic differences existed between the derived and the directly measured TVI curves when subject MRK was tested with 19′–diameter stimuli. Subject MRK was more reluctant than the other subjects to make threshold responses, and by her own admission she often responded one stimulus presentation late in the TVC paradigm. If frequency-of-seeing curves are steeper for the TVI paradigm than for the TVC paradigm, then the derived TVI thresholds could be slightly lower than the measured TVI thresholds. The frequency-of-seeing curves probably are sometimes steeper in the TVI paradigm because a test-illuminance step of 0.1 log unit in the TVC paradigm (Δ log T′=0.1) corresponds to a test-illuminance step of 0.1 log unit plus a background illuminance step of 0.1 log unit (Δ log T=0.1,Δ log B=0.1), whereas in the TVI paradigm test illuminance is stepped by 0.1 log unit with background illuminance held constant (Δ log T=0.1,Δ log B=0).

1999 (1)

1998 (3)

A blood sample from subject MAW was kindly analyzed by Jay and Maureen Neitz using polymerase chain reaction (PCR) methodology to estimate (a) the ratio of LWS/MWS cone pigment genes and (b) the ratio of first to downstream genes.26 Subject MAW had 50% LWS genes and 67% downstream genes. This is consistent with two possibilities: (1) one of her gene arrays has 1 LWS and 2 MWS genes, while the other has 2 LWS and 1 MWS gene, or (2) one of her gene arrays has 1 LWS and 3 MWS genes, while the other has 2 LWS genes. At least 8% of normal males have multiple LWS genes in their single gene array [S. A. Sjoberg, M. Neitz, S. D. Balding, J. Neitz, “L-cone pigment genes expressed in normal colour vision,” Vision Res. 38, 3213–3219 (1998)], implying that at least ∼15% of normal females have multiple LWS genes in one or the other of their two gene arrays.

Baer, S. M.

Balding, S. D.

A blood sample from subject MAW was kindly analyzed by Jay and Maureen Neitz using polymerase chain reaction (PCR) methodology to estimate (a) the ratio of LWS/MWS cone pigment genes and (b) the ratio of first to downstream genes.26 Subject MAW had 50% LWS genes and 67% downstream genes. This is consistent with two possibilities: (1) one of her gene arrays has 1 LWS and 2 MWS genes, while the other has 2 LWS and 1 MWS gene, or (2) one of her gene arrays has 1 LWS and 3 MWS genes, while the other has 2 LWS genes. At least 8% of normal males have multiple LWS genes in their single gene array [S. A. Sjoberg, M. Neitz, S. D. Balding, J. Neitz, “L-cone pigment genes expressed in normal colour vision,” Vision Res. 38, 3213–3219 (1998)], implying that at least ∼15% of normal females have multiple LWS genes in one or the other of their two gene arrays.

If one of subject MAW’s gene arrays has 1 LWS and 2 MWS genes while the other has 2 LWS and 1 MWS gene (see Ref. 27), then the probability of subject MAW being a deutan carrier is less than roughly 49%=0.12/[(0.15)(1-0.12-0.04)+0.12], since ∼12% of women of European ancestry are deutan carriers and ∼4% are protan carriers [L. T. Sharpe, A. Stockman, H. Jagle, J. Nathans, “Opsin genes, cone photopigments, color vision, and color blindness,” in Color Vision: From Genes to Perception, K. Gegenfurtner, L. T. Sharpe, eds. (Cambridge U.P., Cambridge, UK, 1999), pp. 3–51]. If one of subject MAW’s gene arrays has 1 LWS and 3 MWS genes while the other has 2 LWS genes, then the probability of subject MAW being a deutan carrier is 100%. Estimating the overall probability depends on knowing the relative likelihood of the two possibilities.

Nathans, J.

If one of subject MAW’s gene arrays has 1 LWS and 2 MWS genes while the other has 2 LWS and 1 MWS gene (see Ref. 27), then the probability of subject MAW being a deutan carrier is less than roughly 49%=0.12/[(0.15)(1-0.12-0.04)+0.12], since ∼12% of women of European ancestry are deutan carriers and ∼4% are protan carriers [L. T. Sharpe, A. Stockman, H. Jagle, J. Nathans, “Opsin genes, cone photopigments, color vision, and color blindness,” in Color Vision: From Genes to Perception, K. Gegenfurtner, L. T. Sharpe, eds. (Cambridge U.P., Cambridge, UK, 1999), pp. 3–51]. If one of subject MAW’s gene arrays has 1 LWS and 3 MWS genes while the other has 2 LWS genes, then the probability of subject MAW being a deutan carrier is 100%. Estimating the overall probability depends on knowing the relative likelihood of the two possibilities.

A blood sample from subject MAW was kindly analyzed by Jay and Maureen Neitz using polymerase chain reaction (PCR) methodology to estimate (a) the ratio of LWS/MWS cone pigment genes and (b) the ratio of first to downstream genes.26 Subject MAW had 50% LWS genes and 67% downstream genes. This is consistent with two possibilities: (1) one of her gene arrays has 1 LWS and 2 MWS genes, while the other has 2 LWS and 1 MWS gene, or (2) one of her gene arrays has 1 LWS and 3 MWS genes, while the other has 2 LWS genes. At least 8% of normal males have multiple LWS genes in their single gene array [S. A. Sjoberg, M. Neitz, S. D. Balding, J. Neitz, “L-cone pigment genes expressed in normal colour vision,” Vision Res. 38, 3213–3219 (1998)], implying that at least ∼15% of normal females have multiple LWS genes in one or the other of their two gene arrays.

A blood sample from subject MAW was kindly analyzed by Jay and Maureen Neitz using polymerase chain reaction (PCR) methodology to estimate (a) the ratio of LWS/MWS cone pigment genes and (b) the ratio of first to downstream genes.26 Subject MAW had 50% LWS genes and 67% downstream genes. This is consistent with two possibilities: (1) one of her gene arrays has 1 LWS and 2 MWS genes, while the other has 2 LWS and 1 MWS gene, or (2) one of her gene arrays has 1 LWS and 3 MWS genes, while the other has 2 LWS genes. At least 8% of normal males have multiple LWS genes in their single gene array [S. A. Sjoberg, M. Neitz, S. D. Balding, J. Neitz, “L-cone pigment genes expressed in normal colour vision,” Vision Res. 38, 3213–3219 (1998)], implying that at least ∼15% of normal females have multiple LWS genes in one or the other of their two gene arrays.

Although the presence of more than 2 LWS genes is by itself consistent with a substantial probability that subject MAW is color normal (see Refs. 27 and 28), her discrimination data suggest that she indeed is a carrier [J. Pokorny, V. C. Smith, G. Verriest, “Congenital color vision defects,” in Congential and Acquired Color Vision Defects, J. Pokorny, V. C. Smith, G. Verriest, A. J. L. G. Pinckers, eds. (Grune & Stratton, New York, pp. 180–241)]. For females who know that their father and maternal grandfather have normal color vision, and who do not exhibit Schmidt’s sign, the probability of being a carrier is ∼4% (=12%/3). The probability would be less if the color vision of several brothers or maternal uncles were known to be normal. Subject MAW, who did not exhibit Schmidt’s sign, knew the color vision status of only one relative, a color-normal maternal uncle.

If one of subject MAW’s gene arrays has 1 LWS and 2 MWS genes while the other has 2 LWS and 1 MWS gene (see Ref. 27), then the probability of subject MAW being a deutan carrier is less than roughly 49%=0.12/[(0.15)(1-0.12-0.04)+0.12], since ∼12% of women of European ancestry are deutan carriers and ∼4% are protan carriers [L. T. Sharpe, A. Stockman, H. Jagle, J. Nathans, “Opsin genes, cone photopigments, color vision, and color blindness,” in Color Vision: From Genes to Perception, K. Gegenfurtner, L. T. Sharpe, eds. (Cambridge U.P., Cambridge, UK, 1999), pp. 3–51]. If one of subject MAW’s gene arrays has 1 LWS and 3 MWS genes while the other has 2 LWS genes, then the probability of subject MAW being a deutan carrier is 100%. Estimating the overall probability depends on knowing the relative likelihood of the two possibilities.

Sjoberg, S. A.

A blood sample from subject MAW was kindly analyzed by Jay and Maureen Neitz using polymerase chain reaction (PCR) methodology to estimate (a) the ratio of LWS/MWS cone pigment genes and (b) the ratio of first to downstream genes.26 Subject MAW had 50% LWS genes and 67% downstream genes. This is consistent with two possibilities: (1) one of her gene arrays has 1 LWS and 2 MWS genes, while the other has 2 LWS and 1 MWS gene, or (2) one of her gene arrays has 1 LWS and 3 MWS genes, while the other has 2 LWS genes. At least 8% of normal males have multiple LWS genes in their single gene array [S. A. Sjoberg, M. Neitz, S. D. Balding, J. Neitz, “L-cone pigment genes expressed in normal colour vision,” Vision Res. 38, 3213–3219 (1998)], implying that at least ∼15% of normal females have multiple LWS genes in one or the other of their two gene arrays.

Although the presence of more than 2 LWS genes is by itself consistent with a substantial probability that subject MAW is color normal (see Refs. 27 and 28), her discrimination data suggest that she indeed is a carrier [J. Pokorny, V. C. Smith, G. Verriest, “Congenital color vision defects,” in Congential and Acquired Color Vision Defects, J. Pokorny, V. C. Smith, G. Verriest, A. J. L. G. Pinckers, eds. (Grune & Stratton, New York, pp. 180–241)]. For females who know that their father and maternal grandfather have normal color vision, and who do not exhibit Schmidt’s sign, the probability of being a carrier is ∼4% (=12%/3). The probability would be less if the color vision of several brothers or maternal uncles were known to be normal. Subject MAW, who did not exhibit Schmidt’s sign, knew the color vision status of only one relative, a color-normal maternal uncle.

If one of subject MAW’s gene arrays has 1 LWS and 2 MWS genes while the other has 2 LWS and 1 MWS gene (see Ref. 27), then the probability of subject MAW being a deutan carrier is less than roughly 49%=0.12/[(0.15)(1-0.12-0.04)+0.12], since ∼12% of women of European ancestry are deutan carriers and ∼4% are protan carriers [L. T. Sharpe, A. Stockman, H. Jagle, J. Nathans, “Opsin genes, cone photopigments, color vision, and color blindness,” in Color Vision: From Genes to Perception, K. Gegenfurtner, L. T. Sharpe, eds. (Cambridge U.P., Cambridge, UK, 1999), pp. 3–51]. If one of subject MAW’s gene arrays has 1 LWS and 3 MWS genes while the other has 2 LWS genes, then the probability of subject MAW being a deutan carrier is 100%. Estimating the overall probability depends on knowing the relative likelihood of the two possibilities.

Verriest, G.

Although the presence of more than 2 LWS genes is by itself consistent with a substantial probability that subject MAW is color normal (see Refs. 27 and 28), her discrimination data suggest that she indeed is a carrier [J. Pokorny, V. C. Smith, G. Verriest, “Congenital color vision defects,” in Congential and Acquired Color Vision Defects, J. Pokorny, V. C. Smith, G. Verriest, A. J. L. G. Pinckers, eds. (Grune & Stratton, New York, pp. 180–241)]. For females who know that their father and maternal grandfather have normal color vision, and who do not exhibit Schmidt’s sign, the probability of being a carrier is ∼4% (=12%/3). The probability would be less if the color vision of several brothers or maternal uncles were known to be normal. Subject MAW, who did not exhibit Schmidt’s sign, knew the color vision status of only one relative, a color-normal maternal uncle.

A blood sample from subject MAW was kindly analyzed by Jay and Maureen Neitz using polymerase chain reaction (PCR) methodology to estimate (a) the ratio of LWS/MWS cone pigment genes and (b) the ratio of first to downstream genes.26 Subject MAW had 50% LWS genes and 67% downstream genes. This is consistent with two possibilities: (1) one of her gene arrays has 1 LWS and 2 MWS genes, while the other has 2 LWS and 1 MWS gene, or (2) one of her gene arrays has 1 LWS and 3 MWS genes, while the other has 2 LWS genes. At least 8% of normal males have multiple LWS genes in their single gene array [S. A. Sjoberg, M. Neitz, S. D. Balding, J. Neitz, “L-cone pigment genes expressed in normal colour vision,” Vision Res. 38, 3213–3219 (1998)], implying that at least ∼15% of normal females have multiple LWS genes in one or the other of their two gene arrays.

Other (13)

If one of subject MAW’s gene arrays has 1 LWS and 2 MWS genes while the other has 2 LWS and 1 MWS gene (see Ref. 27), then the probability of subject MAW being a deutan carrier is less than roughly 49%=0.12/[(0.15)(1-0.12-0.04)+0.12], since ∼12% of women of European ancestry are deutan carriers and ∼4% are protan carriers [L. T. Sharpe, A. Stockman, H. Jagle, J. Nathans, “Opsin genes, cone photopigments, color vision, and color blindness,” in Color Vision: From Genes to Perception, K. Gegenfurtner, L. T. Sharpe, eds. (Cambridge U.P., Cambridge, UK, 1999), pp. 3–51]. If one of subject MAW’s gene arrays has 1 LWS and 3 MWS genes while the other has 2 LWS genes, then the probability of subject MAW being a deutan carrier is 100%. Estimating the overall probability depends on knowing the relative likelihood of the two possibilities.

Although the presence of more than 2 LWS genes is by itself consistent with a substantial probability that subject MAW is color normal (see Refs. 27 and 28), her discrimination data suggest that she indeed is a carrier [J. Pokorny, V. C. Smith, G. Verriest, “Congenital color vision defects,” in Congential and Acquired Color Vision Defects, J. Pokorny, V. C. Smith, G. Verriest, A. J. L. G. Pinckers, eds. (Grune & Stratton, New York, pp. 180–241)]. For females who know that their father and maternal grandfather have normal color vision, and who do not exhibit Schmidt’s sign, the probability of being a carrier is ∼4% (=12%/3). The probability would be less if the color vision of several brothers or maternal uncles were known to be normal. Subject MAW, who did not exhibit Schmidt’s sign, knew the color vision status of only one relative, a color-normal maternal uncle.

The requisite frequencies for subjects JRC and MRK decreased simultaneously, from 17 to 15 Hz for JRC and from 15 to 13 Hz for MRK. However, the calibration was unaltered. This suggests that some change in the environment (e.g., more light exposure in early springtime) was responsible. The other two subjects were not being tested at the time.

A smaller step size was not used for two reasons. A smaller step size would have increased the duration of the test sessions, which in some cases already exceeded 3 hours. In addition, a smaller step size would have resulted in more-prolonged exposure to suprathreshold flicker.

For each subject, the temporal frequency was chosen to elicit a middle branch. Increasing temporal frequencies by as little as 2 Hz caused flicker thresholds for all temporal contrasts to lie on the equivalent of the upper branch. Reducing temporal frequency caused the range of temporal contrasts corresponding to multiple flicker thresholds to shift to lower temporal contrasts. These results are consistent with previously published data obtained for 13′-diameter stimuli centered within surrounding annuli.4

This was true even for subject JRC (Fig. 3, upper left), for whom the derived and the measured flicker TVI did not share the same set of background illuminances. This disparity resulted from inappropriate corrections to computer lookup tables following a small discrete (1 gear-tooth slippage) rotational translation of the neutral density wedge in the test channel.

This observation was made on the basis of many between-session comparisons for subject JRC and two within-session comparisons for subject MRK. Subject JMG could not serve as a subject for experiments involving the exchange procedure because alternating the short- and long-wavelength lights caused her to become dizzy.

When a 3.26-log-td exchange stimulus was used, light-level limitations precluded measurement of the reappearance threshold.

At background illuminances where the 660-nm flicker TVI curve rises steeply, the time-averaged 540-nm:660-nm test/background combination is metameric to a wavelength appreciably less than 600 nm. For subject JRC, the 660-nm:540-nm log threshold difference typically overshot the MWS-cone isolation line at background illuminances corresponding to the onset of the upper branch of the 660-nm TVI curve. At higher background illuminances, the 660-nm:540-nm differences retreated to values similar to those in Fig. 7. Subject JRC was tested at 17 Hz. (His data are not graphed because the period between test wavelength changes was less than 3 min whenever background illuminance was unchanged). A temporary overshoot would be expected if there were a narrow range of background illuminances for which MWS-cone-mediated flicker response were isolated using 660-nm tests but for which LWS-cone-mediated flicker response continued to predominate with 540-nm tests.

On the basis of data from one subject (JMG), it appears that the 660-nm:540-nm log-threshold difference depends on temporal frequency. Overshoots of the MWS cone isolation line (see note 39) seem more likely to occur for 15- or 17-Hz stimuli than for 13-Hz stimuli. In addition, there was evidence that the slope of the 660-nm:540-nm log-threshold difference versus background-illuminance curve tended to increase as temporal frequency increased from 13 to 17 Hz. The asymptotic 660-nm:540-nm log-threshold differences may have increased also. For subject MAW, who was tested at 14 Hz only, the degree of MWS-cone isolation appeared incomplete. At dim background illuminances, subject MAW’s 660-nm:540-nm log-threshold difference sometimes appeared to be dominated by LWS cones and sometimes appeared to be better described by V(λ).

It is not known why small but apparently systematic differences existed between the derived and the directly measured TVI curves when subject MRK was tested with 19′–diameter stimuli. Subject MRK was more reluctant than the other subjects to make threshold responses, and by her own admission she often responded one stimulus presentation late in the TVC paradigm. If frequency-of-seeing curves are steeper for the TVI paradigm than for the TVC paradigm, then the derived TVI thresholds could be slightly lower than the measured TVI thresholds. The frequency-of-seeing curves probably are sometimes steeper in the TVI paradigm because a test-illuminance step of 0.1 log unit in the TVC paradigm (Δ log T′=0.1) corresponds to a test-illuminance step of 0.1 log unit plus a background illuminance step of 0.1 log unit (Δ log T=0.1,Δ log B=0.1), whereas in the TVI paradigm test illuminance is stepped by 0.1 log unit with background illuminance held constant (Δ log T=0.1,Δ log B=0).

For a test size of 1.1° and luminance of 30 cd/m2, MAW’s R/G ratio Rayleigh matching range was 0.19 log unit. This was obtained by using an anomaloscope with R=649 nm, G=546 nm and Y=588 nm.

Figures (7)

The graph on the right is an idealized two-branched flicker TVI curve. The abscissa represents the background illuminance B, and the ordinate represents the time-averaged test illuminance T of the flickering test stimulus (temporal contrast 100%). The graph on the left is the corresponding flicker TVC curve. The abscissa represents the test stimulus’s temporal contrast C, and the ordinate represents its time averaged illuminance T′. Higher contrast is to the right, as indicated by the icons just above the abscissa. On each graph, the region where flicker is invisible is shaded. The vertical line at temporal contrast C0 on the flicker TVC graph projects to the 45° diagonal line on the flicker TVI plot corresponding to that temporal contrast. Thresholds for the appearance, disappearance, and reappearance of flicker are labeled A, D, and R, respectively. The stimulus is portrayed pictorially beneath the graphs, as a combination of nonmodulated background plus flickering test stimulus (100% contrast) on the right, and equivalently as a solitary flickering stimulus of temporal contrast <100% on the left. The equations at the bottom of the figure relate the two stimulus portrayals to each other. The lowermost equation regarding contrast {C} is derived from the equation C=(Imax-Imin)/(Imax+Imin), where Imax and Imin are the illuminances at peak and trough, respectively, of a temporally modulated stimulus.

Top flicker TVC curves for 19′-diameter stimuli. Subject JRC, 17 Hz (left) and subject JMG, 13 Hz (right). Open symbols, thresholds for the initial detection of flicker; black symbols, thresholds for the disappearance of flicker; gray symbols represent thresholds for the reappearance of flicker. Bottom, flicker TVI curves derived from the flicker TVC curves in the top half of the figure. A coordinate pair (log C, log T′) in TVC space corresponds to a coordinate pair [log(1-C)+logT′,logC+logT′]=(logB,logT) in TVI space. Open, black, and gray symbols correspond to those in the top half of the figure.

Comparison of the flicker TVI curves derived from flicker TVC data with the flicker TVI curves that are measured directly (crosses) for 19′-diameter stimuli. Same symbolism for the derived flicker TVI data (circles) as in Fig. 2.

Comparison of the flicker TVI curves derived from flicker TVC data with the flicker TVI curves that are measured directly (crosses) for 1°-diameter stimuli. Same symbolism for the derived flicker TVI data (circles) as in Fig. 2. Light-level limitations precluded the measurement of reappearance thresholds for subject JMG.

Top, flicker TVC curves obtained with the exchange procedure for 19′-diameter stimuli. Bottom, flicker TVI curves derived from the flicker TVC curves in the top half of the figure. Same symbolism as in Fig. 2.

Comparison of the flicker TVI curves derived from flicker TVC data with the flicker TVI curves that are measured directly for 19′-diameter stimuli. All data were obtained by using the exchange procedure. Illuminance of the 490-nm exchange stimulus was 2.96 log td.36 Same symbolism as in Fig. 2.